Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 73: 995-1003, 1992;
8750-7587/92 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scharf, S. M.
Right arrow Articles by Balaban, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scharf, S. M.
Right arrow Articles by Balaban, K.

Journal of Applied Physiology, Vol 73, Issue 3 995-1003, Copyright © 1992 by American Physiological Society


ARTICLES

Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs

S. M. Scharf, L. M. Graver, S. Khilnani and K. Balaban
Department of Medicine, Albert Einstein College of Medicine, New Hyde Park, New York 11042.

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.


This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
L. Chen and S. M. Scharf
Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs
J Appl Physiol, April 1, 1998; 84(4): 1289 - 1298.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
S. Katragadda, A. Xie, D. Puleo, J. B. Skatrud, and B. J. Morgan
Neural mechanism of the pressor response to obstructive and nonobstructive apnea
J Appl Physiol, December 1, 1997; 83(6): 2048 - 2054.
[Abstract] [Full Text] [PDF]


Home page
J. Appl. Physiol.Home page
O. P. Mathew
Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure
J Appl Physiol, August 1, 1997; 83(2): 371 - 375.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online